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首页> 外文期刊>Infection and immunity >Activation of macrophages in an experimental rat model of arthritis induced by Erysipelothrix rhusiopathiae infection.
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Activation of macrophages in an experimental rat model of arthritis induced by Erysipelothrix rhusiopathiae infection.

机译：实验性大鼠模型中的巨噬细胞活化，由红斑丹毒丝菌感染引起的关节炎。

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Infection of Lewis rats with Erysipelothrix rhusiopathiae represents an experimental model system of acute and chronic arthritis. We studied here the acute inflammatory phase with respect to stimulation of macrophages and lymphocytes. Intragluteal injection of viable E. rhusiopathiae (10(2) to 10(4) bacteria) rapidly induced generalized inflammation, loss of body weight, hind leg arthritis, and systemic macrophage activation within 2 to 3 days. The same symptoms could also be evoked by injection of dead E. rhusiopathiae. Ex vivo, peritoneal macrophages released large amounts of tumor necrosis factor alpha on day 2 and interleukin-1 on day 3, whereas production of prostaglandin E2 was delayed to days 5 to 7 and appeared to counteract tumor necrosis factor alpha synthesis. The inflammatory response and development of arthritis were strongly dependent on T lymphocytes, as evidenced by the following findings: (i) lymphocytes released lymphokines that activated macrophages to enhanced mediator release; (ii) treatment of rats with cyclosporin A reduced infection-induced macrophage activation; (iii) mitogen-stimulated thymocyte proliferation was enhanced, indicating an infection-induced maturation-differentiation process in the thymus; and (iv) in T-cell-deficient nude rats, a higher dose of bacteria was required for infection, the inflammatory response was less severe, and only mild, but not chronic, arthritis developed. Thus, an E. rhusiopathiae-induced inflammation in rats provides a useful tool to characterize activated macrophages and T lymphocytes during the development of acute arthritis and its transition into the chronic form.
机译：刘易斯大鼠患有红斑丹毒丝菌病菌感染代表了急性和慢性关节炎的实验模型系统。我们在这里研究了关于刺激巨噬细胞和淋巴细胞的急性炎症期。臀内注射活的大肠埃希氏菌（10（2）至10（4）细菌）可在2至3天内迅速引起全身性炎症，体重减轻，后腿关节炎和全身巨噬细胞活化。注射死的风湿性大肠杆菌也可引起相同的症状。离体腹膜巨噬细胞在第2天释放大量肿瘤坏死因子α，在第3天释放大量白细胞介素-1，而前列腺素E2的产生延迟至第5至7天，并且似乎抵消了肿瘤坏死因子α的合成。以下发现证明，关节炎的炎症反应和发展强烈依赖于T淋巴细胞：（i）淋巴细胞释放了活化巨噬细胞以增强介质释放的淋巴因子; （ii）用环孢菌素A治疗大鼠减少了感染引起的巨噬细胞活化; （iii）促分裂原刺激的胸腺细胞增殖增强，表明感染引起的胸腺成熟分化过程; （iv）在T细胞缺乏的裸鼠中，需要更高剂量的细菌来感染，炎症反应较轻，仅发展为轻度而非慢性关节炎。因此，大鼠风湿性关节炎引起的炎症提供了一种有用的工具，可用于表征急性关节炎的发展及其向慢性形式转变过程中活化的巨噬细胞和T淋巴细胞。

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